Hemlock poisoning may refer to poisoning by either poison hemlock (Conium maculatum; see the image below) or plants in the water hemlock family (Cicuta species and Oenanthe crocata). Hemlocks are among the few plants that can cause life-threatening toxicity. In both species, the root contains the greatest concentration of toxin, although all plant parts are toxic.
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Hemlock. Photo by Cornell University Poisonous Plants Informational Database
Both water hemlock and poison hemlock have caused severe poisoning in both humans and livestock. Historically, poison hemlock was reportedly used to execute Socrates, and the Old Testament describes rhabdomyolysis in Israelites who consumed quail fed on hemlock.[1] Poison hemlock causes skeletal deformities in the offspring of livestock that eat the plants during gestation (eg, crooked calf disease in cattle). Fatal toxicity has occurred in children who played with whistles made from hollow stems of poison hemlock.[2, 3]
Although related, poison hemlock and water hemlock toxicity have different pathophysiologies and clinical presentations. With water hemlock toxicity, profuse salivation, perspiration, bronchial secretion, and respiratory distress leading to cyanosis develop soon after ingestion; severe toxicity tends to cause seizures, with death resulting from status epilepticus.[4] Poison hemlock toxicity is characerized by rapidly progressive muscle weakness and paralysis, which may eventuate in respiratory failure.[5]
No antidote is available for either toxin. Gastrointestinal decontamination, if appropriate, and aggressive supportive care are the mainstays of treatment.
Poison hemlock, an exotic species introduced to the United States, is a ubiquitous plant with fernlike properties that may reach a height of 2 meters. Poison hemlock grows in diverse settings, including wooded areas, ditches, and waysides throughout the United States, and may be mistaken for other plants such as fool's parsley (Aethusa cynapium).
Water hemlock is typically found growing in moist habitats, such as drainage ditches, marshes, and near bodies of fresh water. Water hemlock has compound leaves; small white or green flowers; and tuberous, large, hollow roots. Water hemlock may reach a height of 2.5 meters and can also be confused with other plants such as wild carrot, also known as Queen Anne's lace (Daucus carota), poison hemlock (C maculata), pignut, sweet flag, watercress, wild parsnip, wild celery, wild ginseng, and kvanne.[6]
See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and poisonings.
Poison hemlock contains several piperidine alkaloid toxins (namely coniine) that are structurally similar to nicotine. Coniine has direct effects on nicotinic (cholinergic) receptors, both agonist and antagonist. Clinically, initial manifestations include gastritis and CNS stimulation (tremor, ataxia, and seizures). Nicotine activation at autonomic ganglia can cause tachycardia, salivation, mydriasis, and diaphoresis. In severe cases, acetylcholine (nicotinic) receptor antagonism develops. This leads to bradycardia, ascending paralysis, and CNS depression (coma). Death is typically from respiratory failure.
Water hemlock
Water hemlock contains cicutoxin, a potent, noncompetitive gamma-aminobutyric acid (GABA) receptor antagonist. Using a rat model, Uwai et al showed that cicutoxin is an antagonist of GABA-mediated chloride channels.[7] Cicutoxin rapidly produces GI symptoms (nausea, emesis, abdominal pain) typically within 60 minutes of ingestion. CNS excitation leads to tremor and seizures, often refractory to therapy. A single bite of the root, which contains the highest concentration of cicutoxin, has been reported to kill an adult.[6]
No human deaths from hemlock ingestion have been reported to US Poison Control Centers during the past 10 years. Prevalence was low for US livestock.[2, 3]
International
Livestock exposures in New Zealand, South America, Europe, and southern Canada have been reported. Cattle appear to be most vulnerable to hemlock toxicity.
Mortality/Morbidity
Poison hemlock poisoning is potentially lethal with large ingestions. Water hemlock fatalities have occurred following a few bites of the root.[4]
Poison hemlock's human median lethal dose (LD50) is not known. Mortality from poison hemlock ingestion is usually secondary to respiratory paralysis.
Water hemlock had a 30% mortality rate in one series of 86 patients. It is recognized as one of the most toxic plants in North America. Mortality from water hemlock is usually secondary to refractory status epilepticus.
Chemical screening test for alkaloids in plant material provides confirmation of toxicity due to poison or water hemlock. However, a plant specimen (or ingested material) is required, and these tests are not routinely available.
Rapidly assess and correct any life-threatening conditions. Since no antidote exists for either toxin, gastrointestinal (GI) decontamination (if appropriate) and aggressive supportive care are mainstays of treatment for hemlock poisoning. Schep et al provide a concise review of water hemlock poisoning and management.[6]
Secure airway.
Decontaminate the GI tract if timing is appropriate.
If no contraindications exist, gastric lavage may be of limited benefit if performed rapidly after the ingestion.
Administer activated charcoal if the patient is able to protect the airway and presents within 1 hour of ingestion. Ipecac should not be used.
Caution should be exercised in patients exposed to water hemlock because they are at increased risk of having seizures, and can eventually aspirate the charcoal.
Treat seizures with benzodiazepines; use barbiturates if needed.
Provide prophylaxis with water hemlock ingestion.
Benzodiazepines and barbiturates help control agitation and raise the seizure threshold.
Aggressively administer IV fluids for dehydration or rhabdomyolysis.
Replete volume if signs of hypovolemia or hypotension are present.
Correct electrolyte abnormalities.
Administer fluids with sodium bicarbonate for urinary alkalinization if evidence of rhabdomyolysis exists. If using sodium bicarbonate, mixing it in 5% dextrose in water (D5W) is important to limit the amount of sodium load.
Potassium levels should be monitored and corrected as needed.
Administer antiemetics. Many antiemetics may lower the seizure threshold and should be used cautiously.
A regional poison center or a medical toxicologist can assist with patient treatment and potentially with plant identification. The regional poison control center should be contacted (800-222-1222) to discuss optimal management of all known or suspected hemlock poisonings.
Clinical Context:
Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.
For maximum effect, administer within 30 min after ingesting poison.
Clinical Context:
Sedative hypnotic with short onset of effects and relatively long half-life.
Increasing action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.
Monitoring patient's blood pressure after administering dose is important. Adjust prn.
Lorazepam contains benzyl alcohol, which may be toxic to infants in high doses.
Clinical Context:
Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately three times longer than diazepam to peak EEG effects. Thus, the clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.
Can be used to control/prevent seizures and may decrease agitation. Rapid onset of action is advantageous, as is their improved safety profile vs barbiturates.
Clinical Context:
Can be administered orally; in status epilepticus, it is important to achieve therapeutic levels as quickly as possible. IV dose may require approximately 15 min to attain peak levels in the brain. If injected continuously until convulsions stop, brain concentrations may continue to rise and can exceed that required to control seizures. Important to use minimal amount required and wait for anticonvulsant effect to develop before giving a second dose.
If IM route chosen, administer into areas with little risk of encountering a nerve trunk or major artery such as one of large muscles like gluteus maximus, vastus lateralis, or other. Permanent neurological deficit may result from injecting into or near peripheral nerves.
Restrict IV use to conditions in which other routes are not possible, either because patient is unconscious or because prompt action is required.
Daniel E Brooks, MD, Co-Medical Director, Banner Good Samaritan Poison and Drug Information Center, Department of Medical Toxicology, Banner Good Samaritan Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals
Disclosure: Nothing to disclose.
Chief Editor
Michael A Miller, MD, Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine, Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program
Disclosure: Nothing to disclose.
Additional Contributors
David A Peak, MD, Associate Residency Director of Harvard Affiliated Emergency Medicine Residency; Attending Physician, Massachusetts General Hospital; Assistant Professor, Harvard Medical School
Disclosure: Partner received salary from Pfizer for employment.
Acknowledgements
Michael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare
Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society
Water hemlock (Cicuta douglasii). United States Department of Agriculture Agricultural Research Service. Available at https://www.ars.usda.gov/pacific-west-area/logan-ut/poisonous-plant-research/docs/water-hemlock-cicuta-douglasii/. August 13, 2016; Accessed: March 27, 2017.
Poison Hemlock (Conium maculatum). United States Department of Agriculture Agricultural Research Service. Available at https://www.ars.usda.gov/pacific-west-area/logan-ut/poisonous-plant-research/docs/poison-hemlock-conium-maculatum/. August 13, 2017; Accessed: March 27, 2017.
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